65 research outputs found

    Image Analysis of Intractable Epilepsy:18F-FDG PET Scan of the Cortical Dysplasia

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    開始ページ、終了ページ: 冊子体のページ付

    A hysteresis model with dipole interaction: one more devil-staircase

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    Magnetic properties of 2D systems of magnetic nanoobjects (2D regular lattices of the magnetic nanoparticles or magnetic nanostripes) are considered. The analytical calculation of the hysteresis curve of the system with interaction between nanoobjects is provided. It is shown that during the magnetization reversal system passes through a number of metastable states. The kinetic problem of the magnetization reversal was solved for three models. The following results have been obtained. 1) For 1D system (T=0) with the long-range interaction with the energy proportional to rpr^{-p}, the staircase-like shape of the magnetization curve has self-similar character. The nature of the steps is determined by interplay of the interparticle interaction and coercivity of the single nanoparticle. 2) The influence of the thermal fluctuations on the kinetic process was examined in the framework of the nearest-neighbor interaction model. The thermal fluctuations lead to the additional splitting of the steps on the magnetization curve. 3) The magnetization curve for system with interaction and coercivity dispersion was calculated in mean field approximation. The simple method to experimentally distinguish the influence of interaction and coercivity dispersion on the magnetization curve is suggested.Comment: 22 pages, 8 figure

    Transition from localized surface plasmon resonance to extended surface plasmon-polariton as metallic nanoparticles merge to form a periodic hole array

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    W. Andrew Murray, Simion Astilean, and William L. Barnes, Physical Review B, Vol. 69, article 165407 (2004). "Copyright © 2004 by the American Physical Society."We present results of experiments to determine the dispersion of the plasmon modes associated with periodic silver nanoparticle and nanohole arrays fabricated using an extension of the nanosphere lithography technique. Ordered monolayers of polystyrene nanospheres were used as a deposition mask through which silver was deposited by thermal evaporation, subsequent removal of the nanospheres thus leaving an array of metallic nanoparticles. By reactive-ion etching of the nanospheres in an oxygen plasma prior to silver deposition, arrays consisting of particles of increasing size were fabricated. The extremities of the particles eventually merge to create a continuous metallic network perforated by subwavelength holes, thus allowing a study of the particle-hole transition. Combining optical measurements of transmittance and reflectance with information gained using scanning electron microscopy, three separate regimes were observed. For low etch times the samples comprise mainly individual nanoparticles and the optical response is dominated by localized surface plasmon resonances that show no dispersion. As the etch time is increased almost all of the nanoparticles merge with adjacent particles, although many defects are present—notably where some particles fail to merge, a small gap being left between them. The presence of these defects prevents an abrupt structural transition from metallic nanoparticles to a continuous metallic film perforated by an array of nanoholes. The presence of such gaps also results in dispersion data that lack clearly defined features. A further increase in etch time leads to samples with no gaps: instead, a continuous metal film perforated by a nanohole array is produced. The optical response of these structures is dominated by extended surface plasmon-polariton modes

    Features of Idebenone and Related Short-Chain Quinones that Rescue ATP Levels under Conditions of Impaired Mitochondrial Complex I

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    Short-chain quinones have been investigated as therapeutic molecules due to their ability to modulate cellular redox reactions, mitochondrial electron transfer and oxidative stress, which are pathologically altered in many mitochondrial and neuromuscular disorders. Recently, we and others described that certain short-chain quinones are able to bypass a deficiency in complex I by shuttling electrons directly from the cytoplasm to complex III of the mitochondrial respiratory chain to produce ATP. Although this energy rescue activity is highly interesting for the therapy of disorders associated with complex I dysfunction, no structure-activity-relationship has been reported for short-chain quinones so far. Using a panel of 70 quinones, we observed that the capacity for this cellular energy rescue as well as their effect on lipid peroxidation was influenced more by the physicochemical properties (in particular logD) of the whole molecule than the quinone moiety itself. Thus, the observed correlations allow us to explain the differential biological activities and therapeutic potential of short-chain quinones for the therapy of disorders associated with mitochondrial complex I dysfunction and/or oxidative stress

    NQO1-Dependent Redox Cycling of Idebenone: Effects on Cellular Redox Potential and Energy Levels

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    Short-chain quinones are described as potent antioxidants and in the case of idebenone have already been under clinical investigation for the treatment of neuromuscular disorders. Due to their analogy to coenzyme Q10 (CoQ10), a long-chain quinone, they are widely regarded as a substitute for CoQ10. However, apart from their antioxidant function, this provides no clear rationale for their use in disorders with normal CoQ10 levels. Using recombinant NAD(P)H:quinone oxidoreductase (NQO) enzymes, we observed that contrary to CoQ10 short-chain quinones such as idebenone are good substrates for both NQO1 and NQO2. Furthermore, the reduction of short-chain quinones by NQOs enabled an antimycin A-sensitive transfer of electrons from cytosolic NAD(P)H to the mitochondrial respiratory chain in both human hepatoma cells (HepG2) and freshly isolated mouse hepatocytes. Consistent with the substrate selectivity of NQOs, both idebenone and CoQ1, but not CoQ10, partially restored cellular ATP levels under conditions of impaired complex I function. The observed cytosolic-mitochondrial shuttling of idebenone and CoQ1 was also associated with reduced lactate production by cybrid cells from mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) patients. Thus, the observed activities separate the effectiveness of short-chain quinones from the related long-chain CoQ10 and provide the rationale for the use of short-chain quinones such as idebenone for the treatment of mitochondrial disorders

    Hypomyelination with atrophy of the basal ganglia and cerebellum: Follow-up and pathology

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    BACKGROUND AND OBJECTIVE: Hypomyelination with atrophy of the basal ganglia and cerebellum is a recently defined disorder. Only a few patients have been described. We report on 11 additional patients and new MRI findings and provide histopathologic confirmation of the MRI interpretation. METHODS: We reviewed the patients' clinical history and present findings. We scored the MRI abnormalities. The histopathology of one patient was re-examined. RESULTS: The patients' early psychomotor development was normal or delayed, followed by increasing extrapyramidal movement abnormalities, ataxia, and spasticity. Mental capacities were variably affected. MRI showed hypomyelination with, on follow-up, evidence of further myelin loss and variable white matter atrophy. The putamen was small or, more often, absent; the head of the caudate nucleus was decreased in size. In contrast, the thalamus and globus pallidus remained normal. Cerebellar atrophy was invariably present. Histopathology confirmed the myelin deficiency, probably related to both lack of deposition and low-grade further loss. The degeneration of putamen was subtotal. The cerebellar cortex was affected, particularly the granular layer. CONCLUSION: Hypomyelination with atrophy of the basal ganglia and cerebellum is a syndrome diagnosed by distinctive MRI findings. Histopathology confirms hypomyelination, low-grade further myelin loss, subtotal degeneration of the putamen, and cerebellar cortical atrophy. All known patients are sporadic, and the mode of inheritance is unclear
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